Flashcards in Oncology Deck (49)
Dental implications of managing oncology patients: What does head and neck cancer involve?
anything below the base of the skull to the larynx
often need to lease with neurological and gastro if cancer spreads, or skin specialists
most commonly SCC
Dental implications of managing oncology patients: Why do exophytic growth cancers have a better prognosis than endophytic?
They grow out of the body so easier to remove
Endo more aggressive
Dental implications of managing oncology patients: Which two strains of HPV are most linked to HandN
HPV 16 AND 18
Dental implications of managing oncology patients: What are the aims of pre-treatment assessment?
Avoidance of unscheduled interruptions to primary treatment as a result of dental problems
Pre-prosthetic planning/treatment e.g., planning for primary implants/impressions for obturator
Planning for extraction of teeth which are of doubtful prognosis or are at risk of dental disease in the future and are in an area where there would be risk of osteoradionecrosis.
Extractions be carried out as early as possible in the patient journey, but as a minimum, at least 10 days prior to radiotherapy.
Planning for restoration of remaining teeth as required.
Preventive advice and treatment.
Assess potential for post treatment access difficulties e.g., trismus, microstomia.
Dental implications of managing oncology patients: What are the short term treatment side effects?
Mucositis: inflammation and ulceration of the mucosal lining of the oral cavity.
Infection: chemotherapy induced neutropenia makes the patient susceptible to bacterial, viral, and fungal infections. Oral candidal infections are extremely common following chemo or radiotherapy.
Xerostomia: dry mouth resulting from a decrease in the production of saliva as a result of radiotherapy.
Dental implications of managing oncology patients: What are the long term treatment side effects?
Altered anatomy: surgical ablation and reconstruction can cause permanent changes in oral anatomy making prosthetic rehabilitation difficult.
Rampant dental caries: Radiogenic dental caries is thought to be the result of reduced salivary flow as well as possible direct radiogenic damage to the amelodentinal junction by radiotherapy.
Trismus: may be caused by surgical scarring or by radiotherapy induced fibrosis of the masticatory muscles.
Mastication difficulties: if a significant number of opposing pairs of teeth are lost
Osteoradionecrosis: hypovascularity and necrosis of bone followed by trauma induced or spontaneous mucosal breakdown, leading to a non-healing wound.
Xerostomia - Challacombe
IMRT (Intensity-modulated radiation therapy ) - current method of radiotherapy which reduces the risk of xerostomia and may also do for osteoradionecrosis after tx
Dental implications of managing oncology patients: What preventative management for cancer patients is there?
Maintenance of good oral hygiene by effective tooth brushing; flossing daily.
Dietary Advice with regard to caries prevention.
Daily topical fluoride application (2800ppm or 5000ppm fluoride toothpaste) in custom-made trays or brush-on. Daily fluoride mouthrinse.
Daily use of GC Tooth Mousse TM containing free calcium (Aldi greek yoghurt cheap)
Saliva replacement therapy/ use of frequent saline rinses
Jaw exercises to reduce trismus (therabite).
Dental implications of managing oncology patients: What is the aetiology of HN cancer?
Lifestyle - lower immune function, diet, etc
Virus - HPV
Dental implications of managing oncology patients: How do you rehabilitate soft tissue?
Radial forearm flap (RFF);
anterolateral thigh flap (ALT);
flaps based on the scapular/para-scapular axis.
Pedicle tongue flap
Dental implications of managing oncology patients: How do you reconstruct the mandible?
deep circumflex iliac artery flap (DCIA)
Cancer chemotherapy: What are the causes of cancer?
• Environmental exposure
• Tumour suppressor genes
Cancer chemotherapy: What is the treatment for cancer?
• Surgery or
• Radiotherapy - Mainly possible when tumour remains localised at the time of diagnosis.
• Chemotherapy - once cancer metastasizes chemotherapy is required for effective cancer management.
• Chemotherapy is often combined with radiotherapy to allow surgical resection to take place.
Cancer chemotherapy: How do chemotherapy drugs vary?
- chemical composition
- route of administration
- type of cancer targeted
- side effects
Cancer chemotherapy: What are the three types of chemotherapy?
• Primary induction chemotherapy - when it is administered in patients with advance cancer for which no alternative treatment exists. Can be curative in only a small subset of patients who present with advance disease. (i.e. Hodgkin’s and non-Hodgkin’s lymphoma in adults or lymphoblastic leukemia in children).
• Neoadjuvant chemotherapy - in patients with localised cancer for which alternative local therapies, e.g. surgery, exist but which are less than completely effective.
• Adjuvant chemotherapy – as an adjuvant to local therapy such as surgery or radiation. Is effective in prolonging both disease-free and overall survival in patients with different type of cancer (i.e. patients with breast, colon gastric or non-small lung cancer).
Cancer chemotherapy: What is the main goal of antineoplastic agents?
The main goal of antineoplastic agents is to eliminate the cancer cells without affecting normal tissues
In reality, all cytotoxic drugs affect normal tissues as well as malignancies - aim for a favorable therapeutic index.
Cancer chemotherapy: What is the therapeutic index?
A therapeutic index is the lethal dose of a drug for 50% of the population (LD50) divided by the minimum effective dose for 50% of the population (ED50).
Cancer chemotherapy: how do you achieve cure?
a TOTAL CELL KILL must be tried
• Early diagnosis and early institution of treatment
• Combination chemotherapy
• Intermittent regimens
• Adjuvant and neoadjuvant chemotherapy occasionally
Cancer chemotherapy: What is the log-kill hypothesis?
It states that a given dose of chemotherapy kills the same fraction of tumor cells regardless of the size of the tumor at the time of treatment.
Chemotherapeutic agents kill a constant PROPORTION of tumour cell population (first order kinetics), rather than a constant NUMBER of cells, after each dose
• Solid cancer tumours – generally have a low growth fractions thus respond poorly to chemotherapy and in most cases need to be removed by surgery
• Disseminated cancers- generally have a high growth fraction and generally respond well to chemotherapy
Cancer chemotherapy: What do cell cycle specific drugs act on?
action on cells traversing the cell cycle
Cancer chemotherapy: What do cell cycle non specific drugs act on?
sterilize tumour cells whether they are cycling or resting in the G0 compartments.
Cancer chemotherapy: What type of agents are CCNS?
- Form highly reactive carbonium ion
- Transfer alkyl groups to neucleophilic sites on DNA bases - causing cross linkage, abnormal base pairing, DNA strand breakage (reduces cell proliferation)
however Alkylating agents are carcinogenic in nature and can increase the risk of secondary malignancies
Cancer chemotherapy: What are alkylating agents CCNS used to treat?
•Usedtotreatawidevarietyofhematologicandsolidtumour (i.e. ovarian cancer, brain tumours)
• Most of the adverse effects are generally dose-related and occur
primarily in rapidly growing tissues
• Nausea and Vomiting. Antiemetics are often given prior and after alkylating agents dosing
Cancer chemotherapy: What type of alkylating agents are there?
Busulfan (Alkyl sulfuantes)
Mainly used for chronic myelogenous leukemia and other leukemias, lymphomas and myeloproliferative disorders. Controls tumour burden but can not prevents transformation or correct cytogenic abnormalities.
Requires biotransformation to agents that have alkylating or carbamoylating activities. Can cross the blood brain barrier, mainly used to treat brain tumours.
Used in the treatment of various cancers, among them malignant melanoma, Hodgkin lymphoma, sarcoma, and islet cell carcinoma of the pancreas. Mainly given IV, is bioactivated in the liver.
Cancer chemotherapy: how may you develop resistant to alkylating agents CCNS?
• Increased activity of DNA repair enzyme
•Increase metabolic inactivation of the drug
• Decrease influx of the drug
Cancer chemotherapy: What is though tot be the mechanism of action for platinum analogues CCNS?
Form highly reactive platinum complexes
Intra strand and interstrand cross-link
inhibits cells proliferation
Cancer chemotherapy: What are the effects of Cisplatin?
Highly bound to plasma protein
Highly concentrated in kidney, intestines and testes. Mainly used for testicular, ovarian cancer and solid tumours (i.e. esophagus, gastric)
Poorly penetrates the BBB
Extensively cleared by the kidney and slowly excreted in urine
Adverse effects - emesis, nephrotoxicity, peripheral neuropathy and ototoxicit
Cancer chemotherapy: What are antimetabolites CCS?
Act on intermediary metabolism of proliferating cells. Interfere with DNA and RNA growth by substituting for the normal building blocks of RNA and DNA (S phase).
Specifically designed and synthesized based on the knowledge of critical cellular processes involved in DNA biosynthesis
• Folates antagonist (i.e. Methotrexate)
• Purine antagonists (i.e. 6 Mercaptopurine)
• Pyrimidine antagonist (i.e. 5 Fluorouracile)
Cancer chemotherapy: What is the action of methotrexate?
Methotrexate (folic acid analogue)
Binds to the active catalytic site of dihydrofolate reductase (DHFR)
Inhibiting the synthesis of tetrahydrofolate (THF)
Interfering with formation of DNA, RNA and key cellular proteins
Poor brain penetration, remains in tissue longer than folate prolonging the inhibitor effect. Remains unchanged in urine
Cancer chemotherapy: What are the effects of methotrexate?
Cytotoxic, mainly on bone marrow
Immunosuppressive, preventing clonal expansion of B and T lymphocytes